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The effect of hypothalamic lesions on estradiol-induced changes in plasma luteinizing hormone (LH) concentration was studied in ovariectomized ewes. The ewes had stainless steel electrodes chronically implanted in the hypothalamus (HYP), and electrolytic lesions were made within 1 h after the injection of 50 microgram estradial benzoate (EB) i.m. Blood samples were collected at 2--6 h intervals for 30 h after EB, and the plasma was subsequently assayed for LH. None of the lesions produced had any effect on the normal immediate (within 12 h after injection) inhibitory effect of estrogen on LH release. However basal hyothalamic lesions, ranging from the suprachiamatic region back over the optic chiasma down to include the anterior tuberal region, effectively inhibited the normal stimulatory effect of estrogen (12--30 h after injection) on LH release. The results are consistent with the interpretation that, in the normal biphasic LH response to injected estrogen in the ewe, the early inhibition of LH release results from direct inhibition of pituitary sensitivity to endogenous LH-releasing factor (LRF). On the other hand the estrogen-induced LH release which occurs subsequent to this inhibitory phase is principally the result of increased LRF secretion by the HYP.

1. With the aim of producing diabetes insipidus in sheep, electrolytic lesions were placed in the ventral medial hypothalamus immediately posterior to the optic chiasm.2. After formation of lesions, the pattern of urine excretion showed a triphasic response consisting of (i) an immediate diuresis reaching a maximum within 4 days, (ii) an interphase of about 12 days wherein rates of urine flow were normal, and (iii) a final phase of permanent polyuria. With the four sheep used in this work, the time between placement of the lesions and onset of permanent hyposthenuria was 19-22 days.3. In the final polyuric phase, the sheep were unable to concentrate their urine in response to dehydration or to feeding.4. Infusions of arginine vasopressin restored the ability of these animals to excrete urine that was hypertonic to plasma.5. The evidence showed that the hypothalamic lesions were effective in producing permanent diabetes insipidus. It was concluded that anti-diuretic hormone (ADH) has essentially the same function in sheep as it has in other mammalian species; that is, the hormone facilitates the elaboration of hypertonic urine. There was no evidence to suggest that ADH had a special effect on potassium excretion in the sheep.